A2 Edexcel biology Revision notes

March 28, 2018 | Author: minayoki | Category: Immune System, Virus, Antibody, Macrophage, Fever


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SNAB A2 RevisionNotes and Unit 4: Environment Survival Topic 5: On the wild side 4.5.1 A particular species can be identified using the features (the phenotype) which are characteristic to only that species. Species with similar phenotypes are likely to be related to each other. A key of characteristics is used to identify the species Organisms are classified into families according to similarity of features. The families start of large, but rapidly become smaller. This is the basis of a hierarchical classification system Kingdom Phylum Class Order Family Genus Species There are 5 kingdoms Animals, Plants, Fungi, Protoctists, Prokaryotes You need to know the main characteristics of each kingdom Taxonomy: the science of classifying living things. Biodiversity: the variety of life on our planet, measurable as the variety within species, between species, and the variety of ecosystems If two organisms can interbreed to produce fertile offspring they are the same species. If not, they are different species Binomial System: (2 names) Felix catus Genus: tells you what group the species is from (has a capital letter) Italics in print Underlined in hand species: tells you the exact species (small case letter) Distinguishing Characteristics of the Kingdoms Prokaryotes      Microscopic prokaryotic cells (2 - 5m long rather than 10-100m) Lack of a nucleus (DNA in cytoplasm) and possibly plasmids Lack of membrane-bound organelles Presence of 70s ribosomes No cytoskeleton Protoctists   Eukaryotic cell structure Simple body form, either unicellular, filamentous (chains), colonial (ball) or macroscopic (large and visible) The Proctoctist’s kingdom tends to be full of organisms that do not fit into any other Kingdom e.g. algae and yeast Fungi    Heterotrophic nutrition (get food from eating, unlike plants) Made of a network of Hyphae, which form a 3D structure called a Mycelium. (look up Module 1 notes) Call walls containing chitin Plants The distinguishing features of the Plants are;       Multicellular with eukaryotic structure Cell walls containing cellulose Complex body form Photoautotrophic nutrition (make food themselves through P/S) Presence of photosynthetic cells with chloroplasts 2 stages in the life cycle: a diploid spore-producing stage and a haploid gamete-producing stage. Animals The distinguishing features of the Animals are;     Multicellular with eukaryotic cell structure Cells without cell walls Heterotrophic nutrition Highly organised organs and tissues including nervous co-ordination  The only haploid cells Genetic diversity they have are gametes 4.5.2 Individuals in the same species look different (have different phenotypes). This is called variation Variation is caused by; 1. The genotype of the individual (i.e. which alleles they have) 2. The environment Genetic diversity describes the range of different genotypes within a species. If there are few genotypes the genetic diversity is small. If there are lots of genotypes the genetic diversity is large.  Advantages of little genetic diversity Advantages of wide genetic diversity All individuals have a preferential phenotype  Less chance of genetic disease  Less chance of extinction when faced with disease (i.e. some individuals will have a phenotype that allows them to survive)  Environment has less effect on phenotype  Species more likely to survive environment change  Species more likely to colonise  Allows access to more niches, therefore less interspecific competition  Natural selection & speciation can occur Causes of Genetic Diversity: 1. Independent Assortment 2. Mutation 3. Random fusion During meiosis sections of DNA are swapped between homologous chromosomes (pairs of chromosomes). This usually occurs by DNA being improperly copied or damaged. This is caused by the orientation of homologous pairs of chromosomes during metaphase 2 of meiosis Changes in the sequence of bases in codons (mutation) cause genetic variation.4. Crossing Over Independent Assortment = which allele of each pair goes into which gamete. Therefore. Chemicals (mutagens) and radiation can do this. Each gamete is different. by combining different gametes new variation occurs (random fusion). This creates more variation by creating new combinations of alleles (crossing over) . D = Big Leaves. a = Green Stem.5.Dihybrid Cross 4.4 F1 Phenotype: Ecological Sampling Techniques 9:3:3:1 A_B_ : A_bb : aaB_ : aabb Purple & Big : Purple & Little : Green & Big : Green & Little .5. leaves ♂ ♀ Parent’s Phenotype: Purple stem & Big Leaves Purple Stem & Big Leaves Parent’s Genotype: AaDd AaDd Gametes: F1 Genotype: d = little AD Ad AD Ad aD ad aD ad AD Ad aD ad AD AAD D AAD d AaDD AaDd Ad AAD d AAd d AaDd Aadd aD AaDD AaDd aaDD aaDd ad AaDd Aadd aaDd aadd 4. A = Purple stem.3 Dihybrid Crosses are for crosses involving two different genes (2 loci). as well as yielding more data than is needed. which affects the survival of organisms. as well as obscuring zonation patterns for lack of observations. Random Sampling (quadrats placed at randomly generated intervals)  Used where habitat is uniform  Removes observer bias  Used in a large area  Used if time is limited Systematic Sampling (quadrats placed at regular intervals)  Used to show zonation  Used where there is continuous variation  Used to sample linear habitats (e.  Too small an interval can make the sampling time consuming.5  Too great an interval may mean that many species actually present are not noted. Line Transect:  Used where time is limited  Used to visually illustrate how species change along a line Belt Transect:  Produces more data. as well as on the time and effort which can be allocated to the survey. Examples include temperature. which affects the survival of organisms. or samples can be taken at particular points along the line For both line and belt transects. 4.5. gives detail about species abundance down the line as well as range  Shows species dominance down the line What interval should be used? Transects can either be continuous with the whole length of the line being sampled.Biotic Factor: A living variable within the ecosystem. the interval at which samples are taken will depend on the individual habitat. Abiotic Factor: A non-living variable within the ecosystem. and water. a roadside) 2 types of systematic sampling technique. light. Examples include predation. competition. An example of a Named Environment Is the British Rocky Seashore .g. and pollution from excreted waste. substrate. Carries opening nocolour sexout eggs shells for towater bespecies 1released year then in optimum change 5.Abiotic Factors have more effect going up the beach Biotic Factors have more effect going down the beach Abiotic Factors include. HasLong Has a mantle antennal pointed organ beak glands. less temp range. presence of excreted wastes Species living in the Rocky Sea shore Splash Zone: Lichen – can survive dessication & temp variation. predation. Has aaction pair of canine teeth behind main of wave teeth 4. Hasto a adapted radula that through 4. Learn this study 3. food availability. Tolerates 2. interspecific competition. water availability. st survive oftheir 3. Has bladders of N 2 that allow it to float (to Dogwhelk: 2. shells Is creating intelligent a perfect and can fit learn with techniques the can rock Adaptations of Species in trophic levels 4. Young mature off-shore and then move back when mature . Vary in across 5. dessication. but more predation from herbivores and carnivores Lower Shore: Kelp – constant environment. grows slowly. fresh water 1. but is less tolerant to dessication than lichen. Has a specialised holdfast that anchors it for to 1. temperature. that forwhich makes opening allows theshells shell it to and 1. Powerful jaws crush crabs 4. breathe Has natural out anti-freeze of water in its bloodwhich to release lots of sperm into the sea 2. Has fucoxanthin pigments that absorb more 2. rocks Have 4. intense competition from same and other species Limpet: (Shore Common Oystercatcher: Crab: ): Micro-algae Bladderwrack 1. As the Strong stop limpet theclaws legs clamps from snapping tofreezing the allows rock open itit dogwhelk grinds 4. intraspecific competition. 1. Haspicking osmoregulate a radula fish covered out (itnotes of can in the teeth cope water with thatvarying grind the Don’t learn this case study if your teacher gave you reach light) microalgae 2. pH etc Biotic Factors include. usually submerged. Retains water in its gill cavity. aspect. wave action. so breath whilst boring shell. lower light levels.5. salinity) Can shutoff down thethe rock circulation in its legs ifCan you’re desperate 2. Has a grove in itsfor shell that to its 4. requires little nutrient Upper Shore: Black Tar Lichen – can survive long periods without water. Middle Shore: Eggwrack – More water availability. Has a very muscular foot to stop the into conditions males / females Micro-algae Limpet Dogwhelk Crab Blenny Oystercatcher effect light than chlorophyll 3. Has specialised gonads (resceptacles) Blenny: barnacle shells head 3.6 on a different habitat. gills stop bubble and them breathes air cooling through through thebores its whole gills a hole bird andin its 3. salinity. 3. 7 Don’t learn this case study if your teacher gave you notes on a different habitat.5. Learn this study if you’re desperate Light Dependent Step of Photosynthesis .4. Chlorophyll absorbs light (remember chlorophyll is the trap in the bottom of the photosystem) .Light Dependent Step: 1. 8 Light Independent Step of Photosynthesis CO2 GP RuBP ADP + P ATP ATP NADPH ADP + P NADP GALP Glucose There are three steps in the Calvin Cycle. ADP + Pi ATP and NADP + H+ + eNADPH 5. H+ for the reduction of NADP and O 2 which is excreted.5. Chlorophyll emits electrons 3. Electron transport chain uses high energy electrons to power the following conversions. ATP provides the energy for converting CO 2 into glucose and NADPH provides the H for glucose. The purpose of the light dependent step is to produce ATP and NADPH. 1. 4. Carboxylation: RuBP fixes CO2to form GP. Electrons are received by electron carrier proteins in the thylakoid membrane (electron transport chain) 4. This reaction is catalysed by the enzyme Rubisco .2. Water is split (photolysis) to produce replacement electrons for the photosystems. 9 4. A glucose molecule is generated every 6 turns of the Calvin Cycle 4.10 Thylakoid membrane = location of photosystems & electron transport chain Stroma = site of Calvin Cycle & photolysis of water Grana provide large surface area for absorbtion of light . reverting to NADP) 3. Regeneration: Some GALP is converted back into RuBP so the Calvin Cycle can continue. The rest of GALP is converted into glucose in a series of reactions. Reduction: In a series of reactions GP reacts with ATP and NADPH reduced GP to form GALP (by reducing GP the NAHPH itself is oxidised.2.5.5. R is like income tax.e.5. Energy is lost in the following ways. NPP = disposable income: what the plant has to spend after paying tax.NPP = GPP – R NPP = Net Primary Productivity (amount of stored chemical energy the plant has to use for growth. energy still present in excreted materials etc . 4. heat. The plant has to pay “respiration tax” because it can’t photosynthesis at night & not all parts of the plant are capable of photosynthesis. energy still present in egested food. through digestion. in respiration (mostly lost through heat).11 Energy in Primary Consumer Lost energy NPP in plant Lost energy Energy in Sunlight Energy is lost between trophic levels. lost as CO2 etc) Best analogy is a salary. This is directly proportional to biomass) GPP = Gross Primary Productivity (amount of stored chemical energy the plant earns through photosynthesis) R = Respiration (amount of energy lost through respiration. through movement. i. GPP is the amount of stored chemical energy the plant earns through photosynthesis. Soon all / most individuals have the “fit” phenotype and the “unfit” phenotype is eradicated 7. produce fertile offspring) with the original organisms.5. lost in respiration. Over this time new mutations occur.12 Evolution: the idea that one species changes into another over time Natural Selection: Darwin’s suggestion for the process by which evolution might occur Evolution by Natural Selection (Darwinian Evolution) 1. At this point a new species has been produced (speciation) . passes through leaves. There is variation in a species 2. These are the “fittest” 4. they are the best adapted to their environment. reflected light. Energy is lost in the following ways. ~3% is converted into NPP. camouflaged). 5. which give new even better alleles 9. The individuals that survive tend to be those that have alleles which give them a selective advantage in their environment (i. This process continues over many generations 8. Over a few generations the frequency of “fit” alleles increases and the frequency of “unfit” alleles decreases 6. The fittest survive long enough to reproduce and pass their alleles onto the next generation.Of the 100% sunlight energy that reaches plants. More individuals are born than the environment can sustain. light of wavelengths not useful to plants. so some individuals must die. e.e. lost as heat etc 4.g. Over time the mutations accumulate in the phenotype until the organism is unable to reproduce (i. 3.e. This means that the environment determines the phenotype of an organism Law 2: Changes are passed on to the next generation So a blacksmith. He publishes with Wallace who wrote to Darwin to discuss his own ideas about evolution. because he noticed that animal populations grow exponentially and then plateau when they reach the limits the environment can sustain (i. They were very similar to Darwin’s and this prompted Darwin to publish.e. will the bigger muscles be passed onto his children? No. Malthus noticed that the human population was expanding exponentially. the population size is determined by the environment) 1809 Lamarck publishes a mechanism for evolution based on two laws Law 1: Organs / structures grow if they are used.14 Isolation is important for evolution because it decreases the size of the gene pool. This stops new alleles coming in from breeding with original . 1859 Darwin publishes the Origin of species by means of Natural Selection. 4. will grow bigger muscles.5. so Lamarck’s theory is easy to falsify. This works! But.14) because this stops the influx of alleles from outside and allows new mutations to accumulate in the genotype more quickly 4.13 1798 Malthus publishes paper on population growth.5.This process is speeded up by isolation (see 4. He thought that the human population would outgrow its resources and that this would lead to famine and war. Darwin was influenced by this idea.5. who uses his muscles all day. 5. These pioneer plants create conditions for the start of plant growth and so more complex plants like grasses and shrubs begin to colonise the area. not a fact.g.15 Evolution is a theory.. large trees take over.5. You should respect the opinions of other people. but cannot reproduce 4. The large trees represent the climax community because succession stops at this point. start to "normalize" the habitat. but reproduce at different times The species exist in the same area. hybrids are produces but they do not survive long enough to breed Hybrids survive to reproductive age. but do not respond to each other’s courtship behaviour Species coexist. 4. creating rudimentary soil from their dead matter.alleles and speeds the accumulation of new mutations (which is what leads to speciation) The different types of isolation. but there are physical reasons which stop them from copulating In some species. pioneer plants like mosses and lichen. Many people believe that species were created (creationism). but by mechanisms other than Natural Selection.16 Primary succession is the first stage of the ecological succession of plant life from abiotic land with no soil to fully support plant ecosystems (e. Method of isolation Ecological isolation Temporal isolation Behavioural isolation Physical incompatibility Hybrid inviability Hybrid sterility Description The species occupy different parts of the habitat The species exist in the same area. a forest). after a few hundred years. In primary succession. . even if you do not necessarily agree with them. which give way to small trees and finally. Other people believe in evolution. Over time the grass area is colonised by small woody plants. Educating people Research enables scientists to understand the role of a species in an ecosystem. food web.5. Unlike secondary succession. Reintroducing species into the wild 4. R = Red.A good example of primary succession takes place after a volcano has erupted. Parent’s Genotype: Rr 1. F1 Genotype:By understanding the niche. reproductive behaviour. habitat. such as hardwood trees by creating soils and other necessities. E. R F1 Phenotype: r r = white R r 9:3:3:1 A_B_ : A_bb : aaB_ : aabb Purple & Big : Purple & Little : Green & Big : Green & Little . In a small population many alleles are lost between generations because an individual only passes on 50% of their alleles. build up population numbers and maintain genetic diversity. The barren land is first colonised by simple pioneer plants which pave the way for more complex plants.17 Parent’s Phenotype: ♀ Red Red Zoos can play a large roleRr in conserving endangered species by. feeding relationships etc scientists can suggest effective methods of conserving species. Captive breeding programmes are used to reintroduce species to the wild.g. which refers to succession after an environmental disaster (such as a forest fire) primary succession occurs on the geologic timescale. Conducting research Gametes: 2. over thousands of years ♂ 4. Running captive breeding programmes 3. There are no set facts to learn. but depends greatly on the species. the more advanced the species the more difficult reintroduction is. how / where to find shelter. building roads with tunnels under them for badgers. To avoid this studbooks are kept (basically. Often just doing something slightly differently will have a big impact on conserving a species e.5. Wild animals are often introduced to captive breeding programmes to avoid these problems Reintroducing species into the wild has some success. Educating people is essential to conservation. This is because animals need to learn specific behaviours e. This decreases the change of genetic drift and also decreases the change of genetic disease. Feeding the animals in the wild also helps survival rates.g.If the parents only have 2 children and they are both Red (RR) then the r allele has been lost. As a general rule of thumb.g. how to reproduce. This is genetic drift and is a big cause of the loss of genetic diversity in an endangered species. group behaviours. a family tree for the captive animals) so that only non-related animals are bred with each other. There are no set facts to learn.18 If you get a question on this in the exam you’ll need to think.19 If you get a question on this in the exam you’ll need to think. . 4.5. how to hunt. 4. Breeding animals in captive environments that mimic the wild has more success because it allows some of these behaviours to be learned in captivity. then the body cools quickly to ambient temperature. The initial plateau at 37˚C lasts 30 – 60 min.6. After 24hrs a body has usually finished cooling and temperature is no longer useful.g. Temperature is measured using a long thermometer with a wide range. Temperature is usually taken rectally or using an abdominal stab. Immunity & Forensics 4. The rate of cooling depends on the situation the body is found in e.SNAB A2 Revision Notes Unit 4: Environment and Survival Topic 6: Infection. o o o o Body temperature Extent of rigor mortis Level of decomposition Forensic entomology Body temperature: A body cools following an S-shaped (sigmoid) curve. .1 Time of death can be measured using the following factors. Muscles stiffen because they run out of ATP. which favours the growth of anaerobic bacteria Greenish discolouration of abdomen (36hrs)  Spreads across rest of body (36 – 72hrs)  Discolouration darkens to reddish green (36 – 72hrs)  Discolouration darkens to purple-black (72hrs)  Body becomes bloated with gas (one week)  Gas is released. On page 80 of your text book is a little more detail about the sequence of events that causes muscles to run out of ATP. body deflates & shrinks (one week +) . This tends to happen in anaerobic conditions. Small muscles stiffen first and unstiffen last.Clothing – slows cooling Found in water – speeds cooling Found indoors – slows cooling Air movements – speed cooling Extent of rigor mortis: Temperature of body Warm Warm Cold Cold Stiffness of body Not stiff Stiff Stiff Not stiff Approx time since death No more than 3 hrs 3 – 8hrs 8 – 36hrs > 36 – 48hrs Rigor mortis is the stiffening of joints and muscles. Muscles unstiffen because the muscle fibres begin to break down. causing the actin and myosin muscle fibres to stick permanently to each other. bacteria from the gut invade tissues and release more enzymes. Level of decomposition: Autolysis is the break down of body tissues using the body’s own enzymes from the digestive system and from lysosomes After this. it is sometimes possible to work backwards from the pupation date and work out hold the maggots must have been when they were taken from the body. . The presence of wounds. a maggot 3mm long found growing at 28˚C will be roughly 0. mummies) stop it completely.g. the clothing the person was wearing and the combination of gases released during decomposition also have an effect. If maggots are taken from the body. allowed to grow and the time taken to pupate is recorded.Autolysis is increased by mild heat and slowed by intense heat. This works because maggots of different species usually take a fixed number of days to pupate.3 days (8 hrs old) 2. Corpse succession: e. 1. Using the life-cycle of the maggot to identify age 3. Forensic entomology: The insects found in a dead body can help identify time of death in 3 ways. Humidity has a big involvement as well – dry conditions slow autolysis and. If the temperature of the body has remained relatively constant the age of the maggots growing in it can be determined by their starting length and the temperature of the part of the body they grew in.g. in some cases (e. Sample is run on an electrophoresis gel. ninhydrin) fingerprints are revealed. Fingerprints: The skin on fingers. This is usually used when the body is damaged (e.g. Identity papers 2. a corpse from a fire) Genetic Fingerprint: Used because DNA is unique to individuals (except identical twins and clones grown by mad scientists). think about it. Using aluminium powder or protein stain (e. Genetic Fingerprint Identity Papers: This is very obvious. tented arches. Fingerprints 3. The satellites are repeated anything from 5 – 500 times and this produces a unique DNA signature.4. Dental records 4. Fingerprinting process: 1.6.g. Sweat and sebum oil is left behind from our fingers on the things we touch. Genetic fingerprinting looks for the presence of repeated sequences of bases in the non-coding sections of DNA (introns). Dental Records: Can be used to identify age and to identify a person based on their dentist’s record of their teeth. 1. Sample is cut using a restriction enzyme 3. . often using a DNA sample of known length to act as a standardization. The repeated sequences are called satellites and can be 2 – 4 bases long (Micro-satellite) or 5 – 20 bases long (Minisatellite).2 The identity of a dead person can be ascertained by. A sample of DNA is copied using PCR 2. toes etc is ridged into specific patterns (arches. whorls & loops). Fingerprints are unique and can be used to identify people. Succession and forensic entomology also show if the body has been moved. and so on until the body has been reduced to a skeleton.3 Succession on corpses: The idea that as each organism or group of organisms feeds on a body. 4. by the age and specific species living on a corpse. A southern blot is taken 5. This change in turn makes the body attractive to another group of organisms. with different groups of organisms occupying the decomposing body at different times. Assuming the original DNA sample has not been contaminated (by e. it changes the body.6.g. which changes the body for the next group. An X-ray is taken to reveal the location of the bands of DNA The fingerprint is the pattern of bands on the electrophoresis gel.4. how old the corpse is.6. This technique allows you to tell. 4. DNA is labeled using a DNA probe specific to the satellite 6. This is a predictable process. a hair from the pathologist) the fingerprint will be exact.4 A typical prokaryote . As a food reserve . Cell membrane. like eukaryotic membranes.Ribosomes. Made of murein (a protein). Mesosome. Sticking cells together 2. Can be exchanged between different bacterial cells. which can be distinguished by a Gram stain: A: Gram positive bacteria have a thick cell wall and stain purple B: Gram negative bacteria have a thin cell wall with an outer lipid layer and stain pink. Tightly-folded region of the cell membrane containing all the proteins required for respiration and photosynthesis. but are smaller (70s rather than 80s). Same function as eukaryotic cells (protein synthesis). Plasmid. DNA. Capsule (or Slime Layer). Used for. Very small circles of DNA. Thick polysaccharide layer outside of the cell wall. containing non-esential genes. There is no nuclear membrane. Always circular. The region of the cytoplasm that contains DNA. Nuclear Zone. made of phospholipids and proteins. Cell Wall. DIFFERENT from plant cell wall. There are two kinds of cell wall. 1. and not in chromosome form. A rotating tail used for propulsion. without proteins DNA is linear and associated with proteins to form chromatin Ribosomes are small (70S) Ribosomes are large (80S) No cytoskeleton Always has a cytoskeleton Cell division is by binary fission Cell division is by mitosis or meiosis Reproduction is always asexual Reproduction is asexual or sexual A typical virus . As protection against desiccation (drying out) and chemicals. Prokaryotic Cells Eukaryotic cells Small cells (< 5 mm) Larger cells (> 10 mm) Always unicellular Often multicellular No nucleus or any membrane-bound organelles Always have nucleus and other membrane-bound organelles DNA is circular.3. Flagellum. and as protection against phagocytosis (being broken down by a white blood cell). whilst others can range from 20 – 3000nm.000 genes). In addition. Some viruses are about 100nm in diameter. which allows the virus to penetrate the host cell membrane by endocytosis. and can be single or double-stranded. polio & herpes). measles & influenza). The viral genome codes for the proteins required to manufacture the virus. The capsomeres can be arranged into an icosahedral shape (e.Viruses have a wide range of different structures. Influenza. TMV & rabies) or a loose containment structure (e. which contains genetic material.g. some viruses also have an outer membrane envelope. The genetic material is either DNA or RNA. HIV and measles virus all have membrane envelopes. All viruses have a protein coat (the capsid). (ligands) Viral Damage – What do Viruses actually do to us? . The virus genetic material (the viral genome) contains only a few genes.g. or a cylindrical shape (e. from about 20 in the polio virus to more than 200 in the herpes virus (human genome contains ~80.g. The protein capsid is made from identical subunits (called capsomeres). Viruses without lipid membranes may have specialised proteins designed to help inject the viral genome into the cell cytoplasm. viruses have protein ligands on their capsid that attach to ligand receptors on eukaryotic cells. HIV) also inject the enzyme integrase. (i) (ii) (iii) Virus RNA enters host cell Virus may also inject RNA Polymerase into host cell as well. HIV targets helper T cells. which makes a cDNA copy of the viral RNA. Other viruses (e. .Like bacteria. Influenza targets epithelial cells & rabies virus targets specific brain cells). DNA Polymerase: RNA Transcriptase: Integrase: Some viruses target specific tissues (e. Other RNA viruses inject the enzyme Reverse Transcriptase. The virus attempts to get its viral genome into the host cell.g. usually through endocytosis using its lipid membrane. After a virus ligand attaches to a host cell ligand receptor it becomes anchored to the host cell. which helps insert the viral cDNA into the host’s DNA Be sure you can recall what the 3 viral enzymes do. Viral RNA and RNA Polymerase enter host cell nucleus via nuclear pores (iv) Viral RNA is copied in nucleus (v) Viral RNA is transcribed using viral RNA Polymerase (vi) Viral mRNA is translated in the cytoplasm (vii) New Virus proteins formed (viii) Viral proteins associate with copied RNA forming new complete viruses (ix) New viruses leave host cell to infect other cells Viruses that have a DNA code instead of an RNA code often insert their viral DNA into the host cell’s DNA. Poliomyelitis virus targets motor neurones. these host cell may lyse (burst) and die. If lots of new virus is being made.g. The cDNA copy is then inserted into the host cell’s DNA. The body launches an immune response to the TB bacterium. TB begins to reproduce in the lungs. malnutrition. Once the bacteria are dead. or another disease – HIV is a common cause) the TB bacterium breaks out and re-infects the body.6.5 & 4. which damage lung tissue & cause coughing. which kills the bacteria. which eventually leads to death. 7.TB can also spread to the lymph nodes in the body. 13.7) 6. increasing the transmission of the disease. TB bacteria can survive inside macrophages as the cell wall of the bacterium is very thick and waxy and is resistant to the macrophage enzymes.6. When the immune system is weakened (by stress. 3. The inside of the granuloma is starved of oxygen. Macrophages enter the lungs in large numbers. Mycobacterium tuberculosis is inhaled into the lungs in droplets of water & mucus from another person’s lung (droplet infection) 2. 1. The bacteria produce toxins. 4. 11.The bacterium can survive and reproduce inside the macrophage for many years without causing infection. Histamine release and inflammation occur (see 4. The macrophages engulf the TB bacteria in large groups. 5.6 Course of infection for Tuberculosis: Tuberculosis (TB) is caused by the Mycobacterium tubercolusis bacterium. The bacteria reproduce too rapidly for the body to destroy 12. forming a mass of tissue called a granuloma. The lungs are progressively damaged. 8. 10. where it reproduces causing the disease scrofula Course of infection for Tuberculosis: .4.6. the lung heals BUT 9. The disease phase. This can last for many years. At the same time the population of Helper T cells falls rapidly. As the numbers of virus increase and the numbers of Helper T cell fall the immune system becomes weaker and weaker. blood-to blood transfer (tattoos. needle sharing. 2. but the Killer T cells keep the numbers in check. Another problem is that HIV attacks Helper T cells.HIV is the Human immunodeficiency Virus. The virus continues to replicate. piercing & cut-tocut transfer). Once inside the bloodstream an HIV infection occurs in 3 distinct phases. 1. because the immune system is weakened other bacteria and viruses are more likely to infect the person (TB may reactivate at this point) 3. HIV rapidly infects Helper T cells and the virus population increases quickly. which are crucial for activating the B cells and also play a role in activating . through sexual intercourse. The chronic phase. which slows the replication of the virus. However.e. The huge problem with HIV is that it mutates very quickly. HIV virus has a ligand (GP120). Eventually a second pathogen will infect the person (an opportunistic infection) which cannot be fought off. The acute phase. which eventually leads to Acquired Immunodeficiency Syndrome (AIDS) HIV is spread by direct contact i. Once inside the body the viral antigens change and the (already damaged ) immune system can’t keep pace with the changes. which attaches to a receptor (CD4) on the membrane of a type of white blood cell called a Helper T cell. The acute phase ends when the Killer T cells begin to recognise infected Helper T cells and kill them. The person will die quickly from the secondary infection and this is the AIDS disease state. Killer T cells. increasing the blood supply to the area. Dead monocytes and pathogen form pus.6. This causes local oedema (the swelling associated with inflammation). Lysozyme is also made by the skin. and is present in tears Interferon: a protein made by virus-infected cells. It allows monocytes and neutrophils into the infected area. epithelial cells. It blocks RNA synthesis and therefore stops virus replication Phagocytosis: the process in which a pathogen is engulfed and destroyed. Lysozyme: an enzyme that breaks down bacterial cell walls. which engulf and destroy foreign bodies and pathogens. Eventually phagocytes arrive and complete the job. The bacterium is taken into the macrophage by endocytosis and enters the macrophage inside a vacuole. Histamine causes local arterioles to vasodilate. It also causes holes to open between endothelial cells in capillary walls.7 Non-specific immune responses: Inflammation: damaged white blood cells and mast cells release histamine at the site of infection. Lysozyme is made in lysosomes inside phagoctyes and is responsible for digesting engulfed bacteria. . Lysosomes containing lysozyme fuse with the vacuole and digest the bacterium inside. causing them to lyse and die. With low numbers of Helper T cell. 4. Macrophages engulf pathogens using pseudopodia (“fake feet”). the immune system cannot communicate effectively and this increases the ability of HIV to survive in the body. Antibodies (also called Immunoglobulins) are proteins produced by B cellls. tears. Once a pathogen has been engulfed and destroyed MHC proteins inside the Macrophage stick to the pathogenic antigen. T cells. they will trigger an immune response. B cells & Macrophages all have the ability to recognise an antigen and once this has happened.6.8 Pathogens have proteins on their surface that our immune system has learned to recognise as foreign. so it can present the foreign antigen and activate the T and B cells responses. These proteins are called antigens.4. macrophages have the ability to present foreign antigens to T and B cells. lymph. tissue fluid. Antigen-binding site . mucus and milk. In addition to this. They are then incorporated into the cell membrane of the Macrophage. They are found in blood plasma. D & E. This means that a single . The families can be distinguished from each other by slight differences in the constant region of the protein Each antobody molecule contains two pairs of proteins. therefore you have the ability to recognise and react to a million different antigens.Two light chains Each pair of chains is held together by disulphide bridges (hydrogen bonds would be too weak). The variable region of the immunoglobulin protein is what recognises & binds to the antigen. Each variable region is different. There are 5 different families of immunoglobulin molecule in the human body (G.Two heavy chains . hence the name. IgG .also known as -globulin). M. There are over a million different B cells in your body. A.Variable Region Disulphde Bridges Constant Region Each B cell produces a different immunoglobulin molecule which recognises and binds to a specific antigen. . Each immunoglobulin molecule has 2 antigen binding sites and can. therefore. bind 2 antigens at one time. 6.Makes it easier for T cell activation as more antigens are presented in one area 4.or Antibody-mediated immune Response. when viruses invade host .9 There are two different types of Immune Response. which causes pathogens to clump together and form the Antibody-Antigen Complex.antibody molecule can bind to 2 pathogens at the same time. However. Antibody Pathogen Antigen The formation of the Antibody-Antigen Complex is important because it.Stops the pathogen from entering a host cell .Isolates pathogens so they cannot infect other host cells . . . A B NB: Cell-mediated Immune Response Antibody-mediated Immune Response. Isolated viruses do not present antigens and therefore do not trigger either the Cell.Makes it easier for macrophages to engulf & destroy the pathogens. They will respond rapidly if the same pathogen invades the body again. B cells can also be activated by macrophages & Helper T cells. 2.cells. When a macrophage digests a pathogenic cell antigens from the cell membrane get stuck in the . 4. These proteins are recognised as antigens. Cloned T Cells differentiate into Killer. This means that the body can mount an immune response before infection becomes serious Suppresor T Cells: stop the immune reaction after about a week Antibody-mediated Immune Response: 1. Cell-Mediated Immune Response: 1. Competent T Cells recognise a specific foreign antigen using its T cell receptor. Helper. Memory or Suppressor T Cells. which makes holes in the pathogen’s cell membrane causing it to die Helper T Cells: stimulate B cells to start producing antibody and attract macrophages to the site of infection Memory T Cells: remain in the lymph nodes. Killer and Helper Cells migrate to the site of infection Killer T Cells: attach to the infected / foreign cell and release the enzyme Perforin. B cells are recognise a specific foreign antigen using the antibody molecules on their surface. Activated T Cell undergoes rapid mitosis forming a large number of identical clone T 3. viral proteins are expressed which become incorporated into the host cell surface membrane via MHC. because they have the right T cell receptor to recognise the pathogen. Negative feedback works as follows.6. Signal causes action 2.macrophage’s membrane. The activated B cell undergoes rapid mitosis and lots of clone B cells are produced 3. Action has effect 3. Cloned B Cells differentiate into either Plasma or Memory cells Plasma Cells Memory Cells a) Plasma cells antibody.g. Effect removes original E. which specific for one antigen only is b) Antibody is transported via the lymph to the site of infection c) Antibody attaches to the specific antigen d) An antigen-antibody formed Memory Cells continue to secrete antibody for many years. 1. insulin stimulates liver to take up glucose & convert it into glycogen stores .10 Negative feedback systems aim to keep something (e. any B Cells which come into contact with the antigen will then be activated 2.g. blood [glucose] or body temperature) at a constant level. High [glucose] in blood causes insulin release 2. 1. so that if the body is infected by the same pathogen the Memory B cells can produce an instant supply of antibody before the infection becomes serious complex is 4. 3. Body temperature is normal Exercise Body temperature rises Detected by thermoreceptors in hypothalamus Hair erector muscles cause body hairs to lie flat Peripheral arterioles vasodilate Sweat glands release sweat onto skin More heat radiated away from skin Sweat evaporates carrying heat away .5˚C. which is the optimum temperature for human enzymes.6.11 Homeostasis is the maintenance of the body’s internal environment. Body Temperature: Body temperature is carefully regulated to maintain a steady 37. This is carefully controlled by a series of systems. [glucose] falls 4. Sensors (thermoreceptors) in the hypothalamus continually monitor blood temperature and activate warming / cooling processes to keep the temperature as stable as possible. which aim to keep conditions at a stable controlled level. Fever can be induced by many factors. vasoconstriction and the production of thyroxine hormone (which makes respiration less efficient. shivering. therefore producing more heat). The hypothalamus now thinks body temperature is too low and triggers a system of responses which aim to generate heat (thermogenesis) and raise body temperature. However. which elevates the thermoregulatory set point. bacterial toxins. i. which causes fever. The cytokines have hundreds of different roles and many more are yet to be discovered.12 . 4. These mechanisms include.6. How does fever work? All white blood cells communicate with each other and the rest of the immune system using a class of hormones called cytokines.e. One class of cytokine is the hormone interleukin. Pyrogens travel in the blood to the hypothalamus in the brain.Less insulating air trapped next to skin Body temperature returns to normal Tuberculosis bacterium (Mycobacterium tuberculosis) causes fever. They bind to receptors there and trigger a complex set of reactions that lead to the production of PGE2 hormone. increased muscle tone. viral proteins and substances produced by necrotic tissue may also trigger fever. it re-sets the body’s natural thermostat to a higher temperature. The general class of hormones that lead to fever are called pyrogens (interleukin is a natural pyrogen). Outer epidermis layer . There are 2 layers in the epidermis.  Skin  Stomach Acid  Normal Flora  Epithelial cells Skin Adaptations for defence: The skin is made from 2 layers. . A Outer cornified layer.Barrier Mechanisms include.Inner dermis layer The epidermis provides a physical barrier to invading pathogens. composed of compacted dead dry cells filled with indigestible keratin protein (which also forms nails and hair) . The skin also has chemical defence mechanisms. where they are swallowed. which are part of the normal flora of the body. Stomach Acid: Is made from HCl at pH 1 – 2. which form a direct physical barrier preventing pathogen attachment 3. Cilia ‘beat’ in waves. which is a natural antibiotic. Epithelial cells have cilia.sebaceous glands also secrete the enzyme lysozyme. Normal Flora: The skin. . Cilia also beat in the GI tract. This makes the skin acidic . Epithelial cell Adaptations for defence: 1. respiratory tract and gut are covered with commensual bacteria. it is a very effective barrier. which is an oil with pH 3 – 5. site of rapid mitosis and keratinisation. Epithelial cells are closely packed & connected by tight junctions forming a continuous impermeable layer 2. .B Inner Malpighian layer. which helps clear bacteria out of the lungs and into the throat. Ingested bacteria are quickly killed by the low stomach pH and digestive proteases.sweat & sebaceous glands secrete sebum. Lysozyme destroys bacterial cell walls. Commensual bacteria are adapted to live the environment of the skin and the gut and the and compete with invading pathogens for the limited supply of nutrients. The memory cells provide active immunity. which is trapped by cilia. When the Memory B cell is activated by the old antigen it makes large quantities on antibody quickly and kills the pathogen before it can infect us properly. Mucus contains lysozyme 4. which remain in our lymph nodes and wait until we are re-exposed to the same pathogen. Plasma B cells make lots of antibody on re-exposure Antibody made by memory B cells provides active immunity Without immunity the level of antibody produced by plasma cells is much less . Epithelial cells secrete mucus.4. a second exposure to antigen produces a much faster response.13 Both T and B Cells differentiate into Memory Cells. However. and several orders of magnitude higher levels of antibody are produced. When we are exposed to a new antigen it takes us about a week to be able to make new antibody. Mucus also directly prevents pathogen attachment 5.6. it is exactly where it wants to be 3. consisting of barriers.6. So how has TB evolved to beat us? 1. which means that. why do we still get ill? Answer: pathogens are evolving as well. which means it is partially protected against lysozyme 5. It does not kill immediately.14 We have evolved a very effective immune system. when inhaled.Passive Immunity is immunity to a pathogen without Memory cells. which is the most effective method of infection 2. It specifically targets epithelial cells. It has a very thick waxy cell wall. It can occur through antibody injection or from drinking breast milk (breast milk contains high [antibody]) Active Natural Immunity – the process above Passive Natural Immunity – beastfeeding (antibody in milk) Artificial Active Immunity . If we’re so good at fighting infections. This means that it has a large window of opportunity to spread to others 4. So how has HIV evolved to beat us? . It can survive inside macrophages and lie dormant until the immune system is weakened. when it can re-infect. It is spread by droplet infection. non-speficif defence mechanisms and specific ones.vaccination Artificial Passive Immunity – antibody injection 4. 1. It specifically targets Helper T cells 4. 2. Penicillin can be taken in large doses by humans because it has no effect on our cells (we have no cell walls). or by using a pour plate). so it can spread 3. Bacteriostatic antibiotics stop bacteria reproducing.6. It stays in the body for years. A disc of blotting paper is soaked in antibiotic of known concentration and placed in the centre of the plate. they do not kill bacteria Bacteriocidal antibiotics kill bacteria 4. penicillin targets the cell wall and breaks it down.15 Antibiotics work by targeting prokaryotic features not found in eukaryotic cells.6. It is spread by sexual contact. 3. A bacterial lawn is grown on an agar plate (either by spreading the bacteria over the plate.1. e.16 The effectiveness of antibiotics can be measured using a disc diffusion technique. A clear circle of dead bacteria will form around the disc . so it is easily spread 4. It weakens the immune system to increase its chance of survival 2.g. Having a protein which pumps antibiotic out of the cell 3. A bacteria can mutate and develop resistance by. but consider that one E coli bacterium can reproduce to form a colony of 2 million bacteria in two hours. months and years that’s a lot of mutations. 1. Bacteria mutate very easily. That might sound like a small amount. Bacteria become resistant because. 1.g.4. Bacteria develop resistance through mutation. So a mutation in one bacterium can quickly be copied to others. Over weeks. Bacteria have the ability to pass copies of plasmids from one to another (conjugation). The diameter / radius of the circle of dead bacteria is proportional to the effectiveness of the antibiotic 5. one can also compare the effectiveness of an antibiotic with a disinfectant or sanitiser (e.6. . even others in different species. Mutating the structure of the bacterium so that the antibiotic no longer works This problem is very serious.17 Bacteria are becoming resistant to antibiotics. One in every million bacteria contains a mutation. In addition. some of which will be beneficial 2. Phenol coefficient) 4. This can be compared to other antibiotics. Having an enzyme that breaks the antibiotic down 2. as long as the same concentration of antibiotic is used. Bacteria reproduce very quickly (they divide every 20min) so a bacterium with a beneficial mutation will spread quickly 3. 4.e. As soon as a bacterium mutates the rest of the bacteria will be killed off by the latest dose of antibiotic. Methicillin Resistant Staphyloccus Aureus (MRSA) has been named the Superbug.g. another way of targeting prokaryotic SNAB A2 Revision Notes structures without damaging eukaryotic ones) there may well be a global pandemic of resistant bacteria. now the field is open for the mutated bacterium to grow without competition.6. because we have do drugs left that can kill it.e. E. Humans have been reckless with use of antibiotics. tipped against humans. they have viral infections) or to people who don’t bother to complete the course of antibiotic. Unit 5: Energy. There are over 100 different types of antibiotic and in the 40years since their development 4 species of bacterium have developed resistance against all of them. Exercise and Coordination Topic 7: Run for your life 5. 4.18 The evolutionary arms race between bacteria and drug developers is. The use of antibiotics speeds the rise of immunity. 5. at the moment. Unless drug developers discover another branch of antibiotics we’re not currently using (i.7.1 . They are often given to people who don’t need them (i. If a bacterial population is continually exposed to antibiotic all bacteria will die. Each fibre is made from bundles of myofibrils. muscles which cause a limb to retract are called flexors. cylindrical muscle cells.2 Muscles are made from muscle fibres arranged into bundles. Arrangement of myofibrils into a muscle fibre Muscle cells (Myofibrils) . the pairs are called antagonistic pairs.Cartilage: a tissue made from collagen. One muscle produces the opposite movement from the other muscle. which are extremely long. Muscles which cause a joint to extend are called extensors. which protects bone ends A muscle: an organ that produces movement by contraction A joint: the junction between two bones A tendon: joins muscle to bone A ligament: joins bone to bone to stabilise a joint Muscles work in pairs. therefore.7. A Synovial Joint Bone Ligament Muscle Cartilage Synovial Fluid Synovial membrane Tendon 5. This is called striation. muscle cell takes on a characteristic banded appearance because of the regular 5.thin Thefilament. A nerve impulse arrives at the neuromuscular junction 2. New ATP binds & the myosin head & causes the myosin head to detach from the actin. protein move position in the thin filament 6. Myosin heads of the thick filament stick to actin Cross-Bridge Cycling: The8. The9. Troponin protein and Tropomyosin arrangement of the sarcomeres. 12. The head rebinds further up the myosin. Note the striated on the thin filament appearance of the muscle 7. sarcomere overlapping ATP (alreadycontains bound to the myosin head)myosin. 14. The myosin head re-cocks 13. actin the thin As the is.sarcomere. Myosin binding sites are exposed A sacromere. Muscle cells Ca2+ bids to Troponin protein in the contain many sarcomeres arranged in parallel. is hydrolysed causingisthe actin and The myosin often headfilament to pivot forwards called myosin the thick because inthe powerstroke myosintheheads make it appear thick. headtherefore.Muscle Fibre 1. The muscle cell is depolarised 3. 10. Ca2+ is released from the sarcoplasmic reticulum inside muscle cells The functional unit of contraction is the4. ADP diffuses away from the myosin head leaving the ATPbinding site empty 11. It is how muscles contract. Repeat stages 7 to 13 until the [Ca2+] falls too low. when contraction stops . pivots the thick filament filament moves across the thin filament – muscle contraction The process by which the thin filaments are pulled in towards each other by occurs the myosin is called cross-bridge cycling. These phosphates are the key to the activity of ATP Adenine base 3 x phosphate Ribose .7. .Ribose (the same sugar that forms the basis of DNA).Key Point: ATP is required to release myosin from actin.Up to 3 phosphate groups. . . in this case the base is adenine.A base (a group consisting of linked rings of carbon and nitrogen atoms). If ATP levels drop (assuming Ca 2+ is present) the myosin stays attached to the actin and the muscle stays permanently 5. Adenosine TriPhosphate (ATP) is made from three components.3 This is what causes rigor mortis contracted. The ATP is then regenerated by recombining the phosphate and ADP in respiration (or another process e. By breaking the 3rd phosphate from the ATP molecule energy is released. The recycling of ATP is crucial for life. which can be used to power intracellular reactions. For example a runner uses ~84kg of ATP in a marathon (more than their total body weight). yet there are only 50g of ATP in the entire body! This means each that each molecule of ATP has been recycled 1676 times during the race! Adenosine ATP = one adenosine molecule with 3 phosphate groups attached P “Energy rich bond” Less energy rich bond(30.The energy used in all cellular reactions comes from ATP.8kJ/mol) “Energy rich bond” ATP + H2O  ADP + Pi (30.6kJ/mol) How the energy in ATP is liberated: Energy Adenosine ADP P + H2O  AMP + Pi Energy Adenosine P AMP + H2O  Adenosine + Pi . photosynthesis).6kJ/mol) (13.g. as soon as ATP has been converted into ADP + P i it is converted back into ATP using energy from Step respiration. NADH & FADH2 are formed (mitochondria christae) 34 x ATP 6 x H2O The electron transport chain uses the NADH and FADH2 made in previous steps to make lots of ATP . the cycle turns ATP. which is attached to a CoA enzyme to form Acetyl CoA. Some ATP is used to split the glucose molecule in the first part of glycolysis 1 x Pyruvate 1 x CoA 1 x Acetyl CoA 1 x CO2 1 x NADH 3C Pyruvate is split into a 2C molecule. Link Reaction (mitochondria matrix) 3. Glycolysis 1 x Glucose 2 x ATP 2 x Pyruvate 4 x ATP 2 x NADH A 6C glucose molecule is split into two 3C pyruvate molecules. Oxidative Phosphorylation 10 x NADH 2 x FADH2 6 x O2 Respiration 1 x CoA CoA enzyme gives its 2C atoms 1 x ATP to a 4C molecule to form a x CO temporarybond 6C molecule. Oxygen required and Carbon andas CO2 Water are produced as waste products. 1. Respiration: a process2 in which the chemical energy In in a 2 (mitochondria 3 x to NADH steps theinto 6C molecule glucose molecules is used convert 38series ADP of molecules 38 matrix) 1 xis FADH releases the Dioxide two C atoms 2 ATP molecules. Reactants Summary However.eventually re-forming the starting 4C compound. As Respiration occurs in 4 distinct steps. The cycle is then ready to repeat itself.Energy Adenosine Normally. Krebs’ Cycle 1 x Acetyl CoA 4. Products during exercise ADP may be converted into AMP or even Adenosine to provide energy. The remaining carbon atom is used to form CO2 (cytoplasm) 2. 4 Respiration: Step 1 .Glycolysis Glucose Glyceraldehyde Phosphate 2ATPs are required Glyceraldehyde Phosphate 2ATPs are made (4 overall) 1 NADH is made (2 overall) .5.7. Pyruvate levels start to rise… Muscle cells turn pyruvate into lactate to stop rising [pyruvate] from stopping Glycolysis (remember. 2ATPs are required for this to happen. In the process of converting one Glyceraldehyde Phosphate to one Pyruvate. Overall.Pyruvate Pyruvate Glycolysis takes place in the cytoplasm of a cell In Glycolysis a Glucose molecule (6C) is split into 2 molecules of Glyceraldehyde Phosphate (3C). This means [NAD] falls. enough energy is released to convert one NAD molecules into one NADH molecules and also to make two ATP molecules. enzyme controlled reactions are reversible and depend on [reactants] and [products]). In anaerobic conditions [H+] rises in the mitochondria as there are no available oxygen molecules to mop it up with and form water. Then. Net gain: 2ATP and 2NADH Pyruvate NADH Lactate NAD . each 3C Glyceraldehyde Phosphate molecule is converted into a 3C Pyruvate molecule. This leads to saturation of the electron transport chain and a build-up of NADH and FADH2. Acetyl CoA levels build-up. 4ATP are made. [CoA] falls and the Link Reaction stops. 2NADH are made and 2ATPs are used. which stops the Krebs’ Cycle. The 2C molecule is attached to a CoA enzyme. Respiration: Step 3 – Krebs’ Cycle Net gain: 2NADH CoA enzyme 2 NADH are made (4 overall) 1 ATP is made (2 overall) 1 FADH2 is made (2 overall) 2 CO2 are made (4 overall) . forming Acteyl CoA.7.5 Overall. 5. which is the basis of the “Oxygen Debt” Respiration: Step 2 – Link Reaction Pyruvate 1 NADH is made (2 overall) 1 CO2 is made (2 overall) CoA enzyme Acetyl CoA Link Reaction takes place in the matrix of the mitochondria In the Link Reaction a Pyruvate molecule (3C) is split into a 2C molecule and a CO2.In the liver the lactate is converted back into pyruvate. therefore the Link Reaction happens twice. 2NADH and 2 CO2 are made. Remember. two molecules of Pyruvate were made at the end of Glycolysis. This requires oxygen. 2CO 2 and 2ATP are made. . The Oxaloacetate can then be used in the cycle again. Oxidative Phosphorylation uses the NADH and FADH 2 produced in the previous steps of respiration to make ATP.6 Respiration: Step 24 – Oxidative Phosphorylation Overall.7. 5. 2FADH . The 6C molecule breaks down into a 4C compound (Succinyl – CoA) releasing enough energy to make one NADH. Succinyl – CoA is converted back into Oxaloacetate and this releases enough energy to make one NADH. one FADH 2 and one ATP. 4NADH. The two spare C atoms are released as two CO2 molecules.Krebs’ Cycle takes place in the matrix of the mitochondria In the Krebs’ Cycle the Acetyl CoA gives its 2C atoms to a 4C molecule (Oxaloacetate) forming an unstable 6C molecule (Citric Acid). therefore the Krebs’ Cycle happens twice. Each NADH makes 3ATP and each FADH2 makes 2 ATP. Remember. two molecules of Acetyl CoA were made at the end of the Link Reaction. Carrier e. . At the end of the Electron Transport Chain. to form water.Carrier ½ O2 + 2H+ ATP FADH 2e - ATP ATP Oxidative Phosphorylation takes place using enzymes embedded in the inner membrane of cristae of the mitochondria Hydrogen atoms from the NADH and the reduced FADH 2 are passed onto 2 the first 2 enzymes of the Electron Transport Chain. which made up the chemical bond between the hydrogen atoms and the NADH / FADH 2 are passed onto 3 Electron Carrier enzymes further down the Electron Transport Chain. Electrons. These enzymes are Hydrogen Carriers and they accept the H atoms from the NADH and the FADH2.Carrier NAD e. This is the only. the electrons are recombined with the H+ atoms and oxygen. but crucial.ATP FADH2 ADP ADP NADH H2O H+ Carrier H+ Carrier e. part of respiration to involve oxygen. Kreb’s Cycle produces. using the energy stored in NADH and FADH2. it generates 2 ATPs Where does the 38 ATP come from? Glycolysis produces. 2ATP Total 2ATP 2NADH 2NADH 6NADH 2 FADH2 4 ATP 10NADH 2 FADH2 Each NADH produces 3ATP  total production is 30ATP from NADH Each FADH2 produces 2ATP  total production is 4ATP from FADH2 Grand Total 4ATP + 30ATP + 4ATP = 38ATP Chemiosmosis of H+ ions from the mitochondrial envelope into the matrix through ATP Synthetase proteins is what actually generates the ATP in respiration The electron transport chain uses the process of chemiosmosis (the diffusion of ions across a membrane). H+ ions are actively pumped into the mitochondrial envelope.NADH starts at the first Hydrogen Carrier and has enough energy to phosphorylate 3ADP. This is done by the proteins in the electron transport chain. . Link Reaction produces. FADH2 has less energy and starts at the second Hydrogen Carrier. H+ ions leave the envelope through ATP Synthetase proteins. The energy is used to pump H + into the mitochondrial membrane against the concentration gradient 3. Whenever an H+ ion moves through the ATP Synthetase protein an ADP is phosphorylated by the ATP Synthetase. Special proteins called ATP Synthetase do allow H+ to pass through them and escape into the mitochondrial matrix.7 In anaerobic respiration lactate is taken via the blood to the liver. where it is broken down into pyruvate using oxygen and NADH.7. NADH and FADH2 contain stored chemical energy 2. 1. The potential energy of the H+ is used to phosphorylate ATP as the H+ moves out of the envelope 5. 5. However. H+ trapped in one place represents a store of potential energy 4. .The [H+] builds up to very high levels in the envelope. H+ cannot escape because it is charged (hydrophilic) and therefore cannot move through the phospholipid bilayer in the envelope membranes. In summary. 7.8 c h e m o r e c e p t o r s in a o r t ic a n d c a r o tid b o d ie s c h e m o r e c e p t o r s in m e d u lla s tr e tc h r e c e p to r s in m u s c le s c o r te x ( v o lu n t a r y c o n t r o l) R E S P IR A T O R Y CENTR E in m e d u lla o f b r a in p h r e n ic n e rv e in t e r c o s t a l n e rv e vagus n e rv e s tr e tc h re c e p to rs in t e r c o s t a l m u s c le s d ia p h r a g m p re s s u re r e c e p t o r s in a o r tic a n d c a r o t id b o d ie s c h e m o r e c e p to r s in a o r t ic a n d c a r o tid b o d ie s te m p e r a tu r e r e c e p to rs in m u s c le s s tr e tc h r e c e p to r s in m u s c le s C A R D IO V A S C U L A R CENTR E in m e d u lla o f b r a in p a r a s y m p a t h e t ic n e rv e ( in h ib it o r ) s y m p a th e tic n e rv e ( a c c e le r a t o r ) s in o a tr ia l node 5.9 v a s o c o n s t r ic tio n and v a s o d ila t io n .5.7. Muscle type in humans is predominantly one or the other due to inherited alleles. You are not expected to know how the spirometer works… although its not very difficult to understand. Therefore. The rate at which the volume decreases is proportionaly to BMR. the total volume will slowly fall as O2 is used. different training programmes can cause the % of either type to change slightly. whereas the muscle of a camel or an elephant will be predominantly slow twitch.10 & 5. The spirometer has fixed volume and is filled with 100% O 2 before the experiment begins. O2 is replaced proportionally with CO 2. BMR can be worked out if a CO2 scrubber is used. However. the muscle type of a cheetah or a gazelle will be predominantly fast twitch. The total volume should stay constant. joggers need slow twitch.7.TV A spirometer is used to plot breathing patterns Vital Capacity: The maximum amount of air a person can exhale after inhaling the maximum possible volume of air Tidal Volume: The volume of air inhaled & exhaled in one breath Basal Metabolic Rate: The rate of respiration The spirometer can be used to plot VC and TV directly. As the person respires. 5. However.11 Sprinters need lots of fast twitch muscle. if CO2 is removed. .7. Increased BMR Decreased blood pressure Increased HDL Decreased LDL . 3. Negative feedback. in this case 37. 1. it is detected. holds systems at a set point. 4.6.Slow twitch fibres Red (lots of myoglobin) Many mitochondria Little sarcoplasmic reticulum Low glycogen content Numerous capillaries Fatigue resistant Fast twitch fibres White (little myoglobin Few mitochondria Lots of sarcoplasmic reticulum Lots of glycogen Few capillaries Fatigue quickly 5. over-training can result in the opposite effect. 2. This is the phenomenon known as “burn-out” Positive effects of exercise include. The thermoregulatory process (and most homeostatic systems) are controlled by negative feedback processes. However.12 See 4. a homeostatic response is activated. If a system changes. 5.5˚C.11 for mechanisms of thermoregulation.13 A moderate level of exercise improves health & well-being. which aims to return the system to its original level.7.7. therefore. This decreses immune response. Tendinitis 9. the patient recovers quickly. Decreased risk of diabetes 7. Phagoctyes and B & T Cells.5. Decreased adrenaline levels 10.Less stress 11. which secrete apoptosis-inducing chemicals in response to non-specific viral or cancerous threat Negative effects of exercise (over-training) include. Decreased risk of CHD 12. Increased muscle inflammation 3.Moderate exercise increases levels of Natural Killer cells. Improved well being 9. Damaged cartilage 8. remote operated tools to repair the damage.7. Because the incisions are small and only the damaged area is targeted.Swollen bursae 5. Increased adrenaline levels 5.14 Key-hole surgery is a technique which allows doctors to conduct surgery with the minimum possible damage to the patient. 2. Decreased levels of Natural Killer Cells. There is also less chance of infection. Muscle tears and sprains 4. If required. Increased cortisol levels. Increased bone density 8. The surgeon makes a small incision (a “key-hole”) and uses a fibre-optic camera to view the damaged area. Ligament damage 10. which also decreases the immune response 6. the surgeon can make a second incision and use a number of small. . Maintaining healthy BMI 6. 1. Increased stress 7. liver damage and kidney damage. re. acne. power of muscles and decrease recovery time Testosterone Binds to androgen receptors Muscle mass increases.7. shrunken testicles Why should we allow use of drugs. which in target cells and increases makes the athlete more transcription of anabolic powerful.      Gives people a chance to be as good as their potential allows Removes “unfair” genetic advantages Controlled use of drugs is less risky People should have the right of choice Legalising drugs makes their distribution controllable (no use by under-age. infertility.should increase the maximum generating ATP. Creatine Creatine combines with Because ATP is re-generated phosphate to form Creatine without using the respiratory Phosphate (CP). This increases the level of work the body can sustain through aerobic respiration (aerobic threshold). such as actin & myosin. infirm etc) Arguments for not using drugs. cells. decreased sex drive.15 Drug Effect on physiology Effect on performance Erythropoietin EPO causes the bone marrow Extra blood cells mean the (EPO) to generate extra red blood blood can carry extra oxygen. the procedure requires a high degree of training. including sports. theoretically it phosphorylate ADP. Side-effects Increased haemocrit increases blood viscosity. skin problems.Unfortunately. This causes strain on the heart and can lead to infarction Diarrhoea . Prosthetics allow people with amputations to participate in many activities. Agression. It also decreases proteins (growth proteins) recovery time. vomiting. 5. CP can pathways.  Dangerous (obviously)  May be pushed onto athletes by trainers  Effects are permanent . expensive equipment and can only be used on certain types of surgery. logical arguments. just think for yourself in the context of the question. Not used under doctor’s supervision  Often cut with other drugs  Exposes athletes to criminals (danger of using other drugs) The list goes on. You can argue the toss either way. but make sure you can back up your opinion with some sensible. . 5.8.8. Exercise and Coordination Topic 8: Grey matter 5.SNAB A2 Revision Notes Unit 5: Energy. Also relays message to the brain.2 . Schwann cells: wrap around the axon of the long nerves. which insulates the nerve and allows for much faster conduction speed.1 Sensory nerve: carries electrical message from receptor to spine Motor nerve: carries electrical message from spine to effector Relay nerve: connects sensory and motor nerves. creating a thick layer of membrane. The thick layer of membrane has gaps in it between adjacent Schwann cells. these are called Nodes of Ranvier. Low light intensity High light intensity Circular muscles: contracted Radial muscles: relaxed Pupil diameter: small Circular muscles: relaxed Radial muscles: contracted Pupil diameter: large 5. .8.3 The Action Potential Voltage-Gated K+ Channels open Voltage-Gated Na+ Channels open Nerve is hyperpolarised and inactive (refractory period) Sequence of events in an action potential. The nerve is ready to fire again As one part of the nerve fires off. Voltage-gated Na+ Channels open 4. A stimulus depolarises the nerve to threshold (-50mV) 3. 5.4 A synapse is the junction between two nerves. Nerve is at resting membrane potential (-70mV) 2. Voltage-gated K+ Channels open 6. Sodium floods into the cell and the membrane potential depolarises to +30mV 5. The 3Na+/2K+ ATPase (Na+/K Pump) concentrations restores the ion 9. one nerve synapses with another (meaning. passes a message to another). The nerve is in the refractory period and cannot conduct another action potential 8. This sequence is repeated like a tiny Mexican wave down the axon of the nerve. This causes the action potential to “jump” between nodes of ranvier.e. i. Na + diffuses into the next section of the nerve.8. When one node depolarises it induces the next section of the nerve to depolarise by forming a mini-circuit between nodes. making conduction speed much faster. which depolarises the nerve to threshold. The neurotransmitter on your syllabus is Ach. Potassium floods out of the cell and the membrane potential falls to -90mV 7. but over 2000 other transmitters have been discovered . Nodes of Ranvier speed this conduction process up.1. It is also a verb. 3 1 2 4 5 7 6 1. The wave of depolarisation arrives at the synaptic knob. The membrane in the presynaptic neuron is depolarised to –50mv (threshold potential) and the voltage-gated Na + channels open, letting Na+ into the cell. 2. The membrane is depolarised to +30mV and voltage-gated K + channels open. The membrane potential falls to –90mV and the cell goes into its refractory period, where the 3Na +/2K+ATPase restored the ion concentrations. 3. Unlike axons, presynaptic nerves also contain a Voltagegated Ca2+ channel. As the presynapstic membrane depolarises these channels open and let Ca2+ into the cell. 4. The Ca2+ causes vesicles in the presynaptic nerve to migrate and fuse with the presynaptic membrane, where they spill neurotransmitter chemical into the synaptic cleft. 5. The neurotransmitter (Acetyl Choline) diffuses across the cleft and binds to receptors on the postsynaptic membrane. 6. The receptors let a little Na+ into the postsynaptic neuron, which is enough to initiate another action potential in the postsynaptic nerve. 7. The ACh is broken down by an enzyme called Acetyl Choline Esterase (AchE), which allows the postsynaptic receptors to be freed ready for a second synapse. In a neuromuscular junction the sequence of events in the synapse is exactly the same. The only difference is that the posysynaptic nerve is a muscle cell and, instead of being flat, the postsynaptic membrane has deep grooves (t tubules) which allow the depolarisation to spread quickly through the muscle so all parts of the muscle contract at the same time. Some neurotransmitters can hyperpolarise postsynaptic nerves, which essentially switches them off. An example of this type of inhibitory neurotransmitter is GABA 5.8.5 Visual transduction is the process by which light initiates a nerve impulse. The structure of a rod cell is: The detection of light is carried out on the membrane disks in the outer segment. These disks contain thousands of molecules of rhodopsin, the photoreceptor molecule. Rhodopsin consists of a membrane-bound protein called opsin and a covalently-bound prosthetic group called retinal. Retinal is made from vitamin A, and a dietary deficiency in this vitamin causes night-blindness (poor vision in dim light). Retinal is the light-sensitive part, and it can exists in 2 forms: a cis form and a trans form: In the dark retinal is in the cis form, but when it absorbs a photon of light it quickly switches to the trans form. This changes its shape and therefore the shape of the opsin protein as well. This process is called bleaching. The reverse reaction (trans to cis retinal) requires an enzyme reaction and is very slow, taking a few minutes. This explains why you are initially blind when you walk from sunlight to a dark room: in the light almost all your retinal was in the trans form, and it takes some time to form enough cis retinal to respond to the light indoors. Rod cell membranes contain a special sodium channel that is controlled by rhodopsin. Rhodopsin with cis retinal opens it and rhodopsin with trans retinal closes it. This means in the dark the channel is open, allowing sodium ions to flow in and causing the rod cell to be depolarised. This in turn means that rod cells release neurotransmitter in the dark! However the synapse with the bipolar cell is an inhibitory synapse, so the neurotransmitter stops the bipolar cell making a nerve impulse. In the light everything is reversed, and the bipolar cell is depolarised and forms a nerve impulse, which is passed to the ganglion cell and to the brain. The bipolar cell is no longer inhibited and depolarises 6.8. The ganglion cell is activated. except that they contain the pigment Iodopsin. which is found in 3 different forms.Summary for light. which carries the message to the brain Cones work in exactly the same way.6 . redsensitive. 1. Bleaching occurs and trans retinal is formed 3. 5. The rod is hyperpolarised and stops releasing inhibitory neurotransmitter 5. Trans retinal blocks Na+ channels 4. blue-sensitive and green-sensitive. Photon hits rhodopsin 2. This gives us colour vision. which release hormone into the blood.7 Midbrain Cerebrum Cerebellum Medulla Hindbrain Brainstem .8. 5. The hormone is carried all over the body. It binds to hormone receptors on cell membranes and initiates responses in those cells. .Homeostasis is the maintenance of the internal environment.Hormone responses give responses over weeks – months Hormones are released from glands.Nerve reflexes give immediate responses . Cerebellum . However. which control the initial processing of visual information. much smaller.controls vital ‘housekeeping’ functions. Midbrain: Thalamus – a relay station that carries sensory information from the sense organs to the correct part of the cortex and hypothalamus. blood pressure and peristalsis. (Speech Premotor Auditory motor area)association area Somatosensory Visual association area . like how to ride a bike. learning.e. which control factors like body temperature and blood osmolarity. where the spine joins the brain Medulla . Other animals have roughly similar size hind. Contains homeostatic centres.and midbrains. personality and memory. whether a stimulus is food or a threat) Hypothalamus – receives sensory information from the thalamus. The Superior Colliculi control object tracking.Brainstem – Uppermost part of the spine.e. spatial position and partial recognition (i. or write).” The cortex is very large in humans and is folded to increase the surface area further.controls muscle co-ordination & learns motor programmes (e. their cortex is much. The thalamus contains the Superior Collicului. The hypothalamus is connected to the Pituitary gland and therefore the hypothalamus can stimulate the release of a great number of pituitary hormones Forebrain: Cortex – processes sensory information and controls the body’s voluntary behaviour. i. This is the part of the brain that actually “thinks. such as heartbeat.g. taste.8.plans and organises thought. pain. Also initiates motor commands.8 .(Understanding language) Occipital lobe .processes & interprets information from the eyes Temporal lobe . is involved with short term memory and puts speech together. 5.processes & interprets information from the ears and processes language and the meaning of words Parietal lobe – processes and interprets information about touch. Frontal lobe . pressure. heat and cold. CT Scans show brain structures.Technique Surgery C T Scan MRI Scan fMRI Scan 5. that shows brain activity. This can be fed into a computer. except that the magnetic fields are tuned to excite deoxygenated haemoglobin. . They also only give “frozen” still images. not brain activity. The rays are collected on the other side of the head and their strength measured. such as cancer. which uses the picture to build up a 3D image of the inside of the head As above. which can be detected.8. stroke and oedema. The density of the tissue the Xray passes through decreases the strength of the signal. However. When the fields are switched off. but whether they are active. This shows up all the areas in the brain where oxygen is being used What it allows us to see The patient can tell the doctor what he/she is feeling as the doctor stimulates parts of his/her brain. and therefore. lets us work out what type of tissue is in the brain. This allows the surgeon to ask the patient questions as he operates on their brain Thousands of narrow-beam Xrays pass through the patient’s head from a rotating source. This can tell us a lot about the function of the brain.9 How it works During brain surgery a local anaesthetic is often used. they are very useful for picking up diseases. This is the only technique. Very similar to above. the protons give out a little energy. but the doctor not only knows what the tissues look like. By recording the energy given out by protons we can build up a sequence of thin pictures of the types of tissues inside the brain. Magnetic fields are used to align protons in water molecules in the patients brain. the cells organise themselves into discrete columns. When we are born.8. We live in a “carpentered world” of straight lines and we interpret line B as a corner (therefore larger than it appears. 5. smaller than it appears. which no longer overlap. There is a “critical window” for this to happen (usually before puberty. If we miss the window. Hubel & Wiesel’s experiments prove this.How to process stimuli correctly must be learned. because it must be far away) and line A as a corner (therefore. As we learn to process stimuli. rather than an innate function of the eye / brain. . which proves the illusion is caused by learned visual processing.10 The Muller-Lyer illusion. the columns overlap and are tangled. younger for visual processing). our brains will become “fixed” with tangled columns and won’t be able to process stimuli properly. because it must be close). The cortex is split into column of cells. Lines A and B are the same length. These optical illusions do not work on Zulus. yet look different – why? The answer is that you have learned to process this kind of stimuli in a certain way. 11 Association (classical conditioning): US  UR (Food  Salivation) Over time. which triggers the CR. the animal learns to ignore the CS. The animal learns the bell signals nothing and it ignores the CS totally. This means no neurotransmitter is released. it learns that an action has a certain outcome AO (pushing a level  food) Habituation: If the neutral stimulus is continuously present (not just before the US). This is called habituation. it becomes associated with the US and begins to elicit the same response. until it is no longer enough to trigger vesicles to fuse with the pre-synaptic membrane. which results in no . If a nerve is frequently stimulated. the amount of Ca 2+ that enters the pre-synaptic nerve gradually diminishes. if a neutral stimulus (CR) is played with the US.5. Eventually. This means that the sensory nerve carrying the message of the CS will always lead to the firing of the motor nerve. but all the time. Operant Conditioning: This is very similar to classical conditioning except the animal learns by doing something i. the animal learns CS  CR (Bell  Salivation) Pavlovian conditioning occurs by synapses between nerves growing together.e.8. What Pavlov discovered was that if a neutral stimulus. It is also difficult to explain using neuronal models of learning (i. a chimp balanced a stick on end under a bunch of bananas suspended from the ceiling. Kohler showed that the chimpanzees sometimes used insight instead of trial-and-error responses to solve problems. the dog will salivate every time the bell is rung. then quickly climbed the stick to obtain the entire bunch intact and unbruised (a better technique than the researchers themselves had in mind). Kohler's experiments showed that primates can both see and use the relationships involved to reach their goals. such as a bell is rung just before the food is given for a few occasions. unconditioned. The food is. In another experiment.8. How insight learning occurs is unknown at the moment. the dog has learned that the bell signals food. that the stimulus is ignored.post-synaptic depolarisation. therefore. Insight Learning: In the early 1900s. . therefore. essentially.e. synapses growing together through use) developed through studies on Aplysia. i. the animals discovered that they could stack boxes on top of each other to reach it. even if no food is presented. They also realized that they could use sticks to knock the banana down. The effect is. When a banana was placed high out of reach. a conditioned stimulus and it prompts a conditioned response. This is not learned and is. In this case.e. This type of learning is very difficult to explain using the Pavlovian model of conditioning. Wolfgang Kohler performed insight experiments on chimpanzees.12 Pavlov’s Dogs Pavlov had observed that an unconditioned stimulus causes an unconditioned response. 5. food causes salivation. CS  CR Hubel & Wiesel Permanently blind monkeys? Hubel & Wiesel investigated the critical window. They used monkeys and kittens in their studies Their work permanently blinded some animals and can be argued to be unethical. Group 3 are blindfolded in one eye (monocular deprivation) 3. Test the activity of nerves in the visual cortex in response to stimuli The results:  Monkeys in Group 2 (both eyes blindfolded) had impaired vision . Test the sensitivity of retinal cells 5. Group 1 are the control (no blindfold). Raise monkeys from birth in three groups for 6 months 2. Hubel & Wiesel’s Method: 1.US  UR US + CS  UR Eventually. Group 2 are blindfolded in both eyes. Test the monkeys to see whether they can see using each eye 4. because of events happening in the brain. and does. All could see. which requires stimulus from the eye. is for the greater good Machines like the MRI were unvested using animals. avert unhelpful potential loss of human life Utilitarian argument: Animal testing Animals have rights too. therefore. Animals can’t tell you when they are suffering Animals are often poorly cared for in labs .14 Animals have no informed consent Testing on animals when the potential side-effects are unknown is immoral.8. in some cases.8. Animal testing is. The Conclusion: There is a critical window for visual neural development. If this window is missed the monkey is blind. You need to know about these experiments because they all use animals Clinical Trials Stage 1 involves animals. 5.13 WhyArguments not use computer Arguments Against simulations in Without animals we would notFor be able Clinical trials instead? to discover new drugs Animal physiology is different to human Animal testing is better than nothing physiology. Animal testing has advanced our understanding of human physiology 5.    Monkeys in Group 3 (monocular deprivation) were blind in the deprived eye Retinal cells were responsive in all groups Cortical activity was reduced in parts of the brain that process information from the deprived eye Adults undergoing the same tests showed no difference between groups. not the eye. This binds to protein pumps on the pre-synaptic membrane of nerves that secrete serotonin. which helps alleviate some of the symptoms of the disease.16 Continuous variation: there is a wide range of phenotypes (e. In depression neurons in the brain that secrete serotonin neurotransmitter stop working properly and serotonin levels fall. therefore reducing firing in post-synaptic nerves. In both cases treatments that increase the levels of neurotransmitter might prove successful in relieving the symptoms of these diseases 5.In Parkinson’s disease neurons in the brain die. giving greater post-synaptic activation and a sense of euphoria.8.g. height) Discontinuous variation: phenotypes fall into discrete categories (e. when these channels are blocked. which causes difficulty in movement and limb shaking. serotonin builds up in the cleft.g.8. L-Dopa: This is a precursor of dopamine. BUT. blood type) . All these neurons secrete dopamine neurotransmitter.15 Drugs that affect synapses can drastically alter the functioning of the brain. The pumps would normally take serotonin up after it had been released. MDMA: Active ingredient in ecstasy. 5. When given to Parkinson’s sufferers it is turned into dopamine. which produces the much greater range of possible phenotypes. . with many alleles.17 Brain development is a combination of nature and nurture. usually with an environmental trigger. This is usually coded for by many genes (polygenes).Discontinuous variation tends to be coded for by one gene with a few different alleles. continuous variation is more complex. Polygenes can give rise to susceptibility to disease.8. However. Diseases that are both genetic and environmental are called multifactorial 5.
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